“Diabetes mellitus” (or diabetes) is one of the most prevalent diseases in the world today. Individuals suffering from diabetes have been divided into two classes, namely type I or insulin-dependent diabetes mellitus and type II or non-insulin-dependent diabetes mellitus (NIDDM). Non-insulin-dependent diabetes mellitus (NIDDM) accounts for approximately 90% of all diabetics, and is estimated to affect 12 to 14 million adults in the United States alone (6.6% of the population). NIDDM is characterised both by fasting hyperglycaemia and exaggerated postprandial increases in plasmatic glucose levels. NIDDM is associated with a variety of long-term complications, including microvascular diseases, such as retinopathy, nephropathy and neuropathy, and macrovascular diseases, such as coronary heart disease. Numerous studies in animal models show a causal relationship between long-term complications and hyperglycaemia. Recent results obtained by the Diabetes Control and Complications Trial (DCCT) and the Stockholm Prospective Study have for the first time demonstrated this relationship in man by showing that insulin-dependent diabetics have a substantially lower risk of development and progression of these complications if they are subjected to tighter glycaemic control. Tighter control is also expected to benefit NIDDM patients.
Hyperglycaemia in the case of NIDDM is associated with two biochemical anomalies, namely insulin resistance and insufficiency of insulin secretion.
The initial treatment of NIDDM is based on a controlled diet and controlled physical exercise, since a considerable number of diabetics are overweight or obese (˜67%) and since loss of weight can improve insulin secretion and sensitivity to insulin and lead to normal glycaemia.
Patients suffering from hyperglycaemia that cannot be controlled solely by diet and/or physical exercise are then treated with oral antidiabetics.
Several categories of oral antidiabetics are currently used in monotherapy for the treatment of NIDDM:                insulin secretion stimulators. They are represented, firstly, by sulfonylureas (SU) and by “glinides”. As regards SUs, mention will be made in particular of carbutamide (Glucidoral®), glibenclamide/glyburide (Daonil®, Euglucan®), glibomuride (Glutril®), gliclazide (Diamicron®), glimepiride (Amarel®) and glipizide (Glibenese®). As regards the “glinides”, mention will be made in particular of repaglinide (NovoNorm®);        agents that reduce glucogenesis, represented by the biguanides. Mention will be made in particular of metformin (Glucophage®, Stagid®);        insulin sensitisers, represented mainly by thiazolidinediones (TZD). Mention will be made in particular of pioglitazone (Actos®) and rosiglitazone (Avandia®);        alpha-glucosidase inhibitors. Mention will be made in particular of acarbose (Glucor®) and miglitol (Diastabol®).        
However, the monotherapy may show a loss of efficacy over time. This is referred to as “secondary deficiency”. This may represent up to 50% unsatisfactory response after 10 years of treatment. The studies conducted have shown that it is possible to deal with this problem by combining in the same pharmaceutical form metformin with sulfonylureas or TZD (EP 869 796 B1, EP 974 365 B1, EP 861 666 B1, WO 03/006004 A2), and a number of these fixed combinations have been marketed:                metformin+glibenclamide/glyburide (Glucovance®)        metformin+glipizide (Metaglip®)        metformin+rosiglitazone (Avandamet®).        
Triazine derivatives with an antidiabetic effect comparable to that of metformin have been described in WO 01/55122.
The applicant has demonstrated, entirely unexpectedly, that the combination of an antidiabetic agent of triazine type, such as those described in WO 01/55122, and of an insulin secretion stimulator shows a synergistic effect and a very strong decrease in side effects compared with metformin combinations, especially as regards nausea and diarrhea.